Effect of carbon dioxide on the activity of slowly and rapidly adapting pulmonary stretch receptors in cats.

Single fiber activity from slowly and rapidly adapting pulmonary stretch receptors (PSR) was recorded from the left cervical vagus of anesthetized, open-chested and artificially ventilated cats. Reducing the end-tidal CO2 to low values did not affect the frequency of occurrence of higher threshold (HT) PSR. Occlusion of the left pulmonary artery (LPA) had no significant effect on the resting discharge of both HT and low threshold (LT) PSR. Cyclic ventilation with 8% CO2 in O2 reduced the activity of LT and HT receptors by similar amounts, irrespective of their anatomical location. After LPA occlusion, CO2 ventilation reduced markedly the activity of both type of PSR but to the greatest extent that of the HT receptors, the majority of which were located in the intrapulmonary airways. The CO2 depressant effect may not be due solely to changes in H+ concentration at the receptor level, since acetazolamide did not totally abolish the effect even though it significantly reduced it. Sustained inflation with 8% CO2 in O2 significantly reduced the activity of HT receptors in both the dynamic and static phases of inflation, but had no effect on the activity of LT receptors. Direct localization showed that the receptors which were more accessible to CO2 (all HT and one LT) were located in the lung parenchyma. In the case of rapidly adapting receptors, sustained inflations with CO2 gave inconsistent results. The results show clearly that, as in other mammalian species, the PSR activity in cats is also reduced by hypercapnia. The present study stresses the importance of localizing the PSR and making the observations separately on the two types of PSR, for there may be qualitative and quantitative differences.